Dementia is a syndrome of progressive, irreversible cerebral dysfunction caused by structural neropathologic alterations and characterized by cognitive functional loss. The condition is characterized by a slow disintegration of personality and intellect due to impaired insight and judgement. Alzheimer-type dementia is due to a degenerative process, the most prominent early symptom being memory loss. Alzheimer3 s presenile dementia typically begins in the fifties and sixties; senile onset dementia begins in the seventies and eighties. The dementia usually progresses steadily, becoming well advanced in two or three years.
Vasoactive intestinal peptide, or VIP, is reported to cause various biological actions in humans and animals. This peptide has actions on the cardiovascular system, where it promotes vasodilation of various vessels, on the respiratory system, and on the endocrine system. In the central nervous system, it provokes an excitation of cerebral-cortical and spinal cord neurons, hyperthermia, and stimulation of glucose utilization. The five-amino-acid (TDNYT) sequence of positions 7-11 of VIP shares homology with the pentapeptide TTNYT of Peptide T (described in more detail below) which interferes with the proposed attachment sequence of the human immunodeficiency virus (HIV). The HIV envelope glycoprotein, gp120, is responsible for viral binding to the T4 molecule. Peptide T inhibits gp120 binding to human T cells and inhibits human T cell infectivity. This suggests the possibility that VIP, or certain fragments of it, are endogenous ligands for the T4 receptor as reported by Sacerdote, Ruff and Pert, Journal of Neuroscience Research, 18:102-107 (1987).
Alzheimer's disease or dementia is believed to be caused by deterioration of the cholinergic neurons in the basal forebrain. Vasoactive intestinal polypeptide is co-localized with cholinergic neurons in most parts of the body, including the cholinergic neurons in the basal forebrain. Vasoactive intestinal polypeptide tends to maintain neuronal survival. In a proposed secondary phase of Alzheimer's disease, endogenous neurons of the cortex of various different chemical types degenerate following deprivation of their vasoactive intestinal polypeptide neuronal growth factor which was once contained in the cholinergic endings.